Rebound phenomenon of inflammatory response may be a major mechanism responsible for increased cardiovascular events after abrupt cessation of statin therapy

• Published in: Medical hypotheses 2006, Vol.66 (6), p.1199-1204
• Main Authors: Li, Jian-Jun, Li, Yi-Shi, Chen, Jue, Yang, Jin-Qi
• Format: Article
• Language: English
• Subjects: Cardiovascular Diseases - chemically induced; Cardiovascular Diseases - epidemiology; Cardiovascular Diseases - immunology; Clinical Trials as Topic; Evidence-Based Medicine; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Models, Immunological; Systemic Inflammatory Response Syndrome - chemically induced; Systemic Inflammatory Response Syndrome - epidemiology; Systemic Inflammatory Response Syndrome - immunology; Withholding Treatment
• ISSN: 0306-9877; 1532-2777
• DOI: 10.1016/j.mehy.2005.06.035

Inflammation has been recognized as having an important role in the development and progression of atherosclerosis. Statins reduce cardiovascular events mainly by cholesterol lowering. A large number of investigations have demonstrated that administration of statin could modify inflammatory response with a concurrent fall in cardiovascular events. Despite the known benefit of statin therapy, many cardiac patients abruptly discontinue therapy because of financial constraints, forgetfulness, or side effects. More recently, several studies have shown that abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. However, the mechanisms of the increased incidence of cardiovascular events after abruptly stopping statin therapy are still unknown. A few data suggest that abrupt withdrawal of statin therapy deteriorates endothelial function, result in expression of pro-inflammatory gene involved in the development and progression of atherosclerosis. We hypothesis that rebound phenomenon of inflammatory response may be a major mechanism responsible for increased cardiovascular events after abrupt cessation of statin therapy. Our very recent data showed that abrupt termination of statin therapy resulted in a rapid increased C-reactive protein (CRP) and interleukin-6 (IL-6) levels in patients with hypercholesterolemia. This finding may be of important interest in the connection between inflammatory response and abrupt withdrawal of statin therapy in patients with coronary artery disease.